Outer hair cells functionally and structurally deteriorate during reperfusion

Tabuchi, Keiji; Tsuji, Shigeki; Fujihira, Kazuya; Oikawa, Keiko; Hara, Akira; Kusakari, Jun

doi:10.1016/s0378-5955(02)00349-0

Cited by 36 publications

(41 citation statements)

References 11 publications

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“…The OHCs of guinea pigs might prove more vulnerable to ischemia/reperfusion injury than IHCs. 24,38 Besides ischemic damage, OHCs in guinea pigs are more vulnerable to other cochlear injuries, such as aminoglycoside ototoxicity. 39 Longer periods of ischemia may affect both IHCs and OHCs.…”

Section: Discussionmentioning

confidence: 99%

Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway

Kao

Tsai

Lai

et al. 2011

Laboratory Investigation

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Aminoglycoside ototoxicity is a common cause of drug-induced hearing loss. Toxicity is dose related, but some patients may still develop hearing loss even under safe dosage. Apart for genetic idiosyncrasy, indirect evidences imply that ischemia may increase the aminoglycoside ototoxic sensitivity because common clinical situations associated with cochlear ischemia such as noise, sepsis, and shock are known to augment the development of aminoglycoside ototoxicity. At present, a direct interaction of cochlear ischemia and aminoglycoside ototoxicity is still lacking. This study demonstrated a direct evidence of increased gentamicin (GM) ototoxic sensitivity in chronic guinea pig models of transient cochlear ischemia. No permanent auditory changes were observed after a single dose of GM (125 mg/kg) or after transient cochlear ischemia for 30 min. Persistent and significant auditory threshold shift was detected when GM was given after transient cochlear ischemia. Cochlear hair cells and spiral ganglion neurons are the major regions affected. Apoptosis contributes to hair cell death during acute interaction of ischemia and GM ototoxicity. Increased apoptotic cell death was also depicted when GM crossreacted with hypoxia in vitro, using cochlear cell lines. Generation of reactive oxygen species, loss of mitochondrial membrane potential, calcium release, and caspase-dependent apoptotic cell death were shown during the interaction of hypoxia and GM ototoxicity in vitro. This synergistic ototoxicity may be critical to aminoglycoside-induced hearing loss in clinical scenarios. The results should improve our understanding of the interacting mechanism and potential preventive strategy to aminoglycoside ototoxicity.

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Section: Discussionmentioning

confidence: 99%

Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway

Kao

Tsai

Lai

et al. 2011

Laboratory Investigation

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“…CAP was recorded at the bony edge of the round window by an Ag / AgCl electrode (8). The reference electrode was placed on the neck muscles.…”

mentioning

confidence: 99%

Dehydroepiandrosterone Sulfate Reduces Acoustic Injury of the Guinea-Pig Cochlea

et al. 2005

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Abstract. The present study was performed to determine effects of dehydroepiandrosterone sulfate (DHEAS), a neurosteroid, on acoustic injury. Albino guinea pigs were exposed to a 2 kHz pure tone of 120 or 125 dB sound pressure level for 10 min immediately after intravenous administration of DHEAS. Statistically significant improvement in the compound action potential threshold shifts and in amplitude reduction of distortion-product otoacoustic emissions was observed 1 week after the acoustic overexposure in the animals treated with DHEAS. The present results suggest that DHEAS has a protective effect against acoustic injury of the cochlea.

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“…Further studies will be necessary to clarify the detailed mechanism of the inhibitory actions of GABA in the cochlea. It has been demonstrated that the excitotoxicity of afferent dendrites plays important roles in cochlear ischemia (Pujol et al 1990 andTabuchi et al 2002) and acoustic injury (Puel et al 1998). Glutamate exicitotoxiciy often causes temporary threshold shifts in this type of injury.…”

Section: Discussionmentioning

confidence: 99%

“…The composition of artificial perilymph used in this study was as follows; 137 mM NaCl, 5 mM KCl, 2 mM CaCl 2 , 1 mM MgCl 2 , 1 mM NaHCO 3 , 11 mM glucose, pH 7.4 (Bobbin et al 1974 andTabuchi et al 2002). For the application disease.…”

Section: Drug Administrationmentioning

confidence: 99%

Activation of the GABAA Receptor Ameliorates the Cochlear Excitotoxicity Caused by Kainic Acid in the Guinea Pig

Sakai

Tabuchi

Murashita

et al. 2008

Tohoku J. Exp. Med.

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Excitotoxicity is a major neurotoxic mechanism in cochlear disorders, including cochlear ischemic injury and acoustic injury. Kainic acid (KA), an excitatory amino acid, can damage glutamatergic neurons. The application of KA to the round window membrane, an opening of the cochlear bony labyrinth to the middle ear, induces excitotoxicity of cochlear afferent dendrites and significantly decreases the amplitude of compound action potential of the cochlea (CAP), a cochlear potential generated by activation of the auditory nerve fibers. On the other hand, muscimol, a gamma-aminobutyric acid (GABA) A receptor agonist, is neuroprotective in excitotoxicity in the central nervous system. Here we studied whether activation of GABA receptor decreased the excitotoxicity of the cochlea caused by KA. KA (10 mM) was applied to the round window membrane of guinea pigs for 30 minutes. Muscimol, bicuculline, a GABA A receptor antagonist, or baclofen, a GABA B receptor agonist, was given at the onset of KA application. The threshold shift of CAP was examined with chronically implanted electrodes. Application of KA significantly elevated the CAP threshold on day 1 and day 3 as compared with the pre-application level. Muscimol significantly decreased the KA-induced CAP threshold shifts. Furthermore, this protective effect of muscimol was inhibited by the application of bicuculline, a GABA A receptor antagonist. However, baclofen, a GABA B receptor agonist, did not affect the CAP threshold shifts caused by KA. These results suggest that activation of GABA A receptor could prevent cochlear excitotoxicity. GABA A rececptor activation may represent an effective treatment of cochlear ischemc injury and acoustic injury.

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Outer hair cells functionally and structurally deteriorate during reperfusion

Cited by 36 publications

References 11 publications

Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway

Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway

Dehydroepiandrosterone Sulfate Reduces Acoustic Injury of the Guinea-Pig Cochlea

Activation of the GABAA Receptor Ameliorates the Cochlear Excitotoxicity Caused by Kainic Acid in the Guinea Pig

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